LiveingWell Health News Letter

1. MANGANESE  2. HEALTH SITES  3.THOUGHT OF THE DAY

1.Manganese

Manganese is a mineral element that is both nutritionally essential and potentially toxic. The derivation of its name from the Greek word for magic remains appropriate because scientists are still working to understand the diverse effects of manganese deficiency and manganese toxicity in living organisms.

FUNCTION

Manganese (Mn) plays an important role in a number of physiologic processes as a constituent of some enzymes and an activator of other enzymes.

Antioxidant function

Manganese superoxide dismutase (MnSOD) is the principal antioxidant enzyme of mitochondria. Because mitochondria consume over 90% of the oxygen used by cells, they are especially vulnerable to oxidative stress. The superoxide radical is one of the reactive oxygen species produced in mitochondria during ATP synthesis. MnSOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which can be reduced to water by other antioxidant enzymes.

Metabolism

A number of manganese-activated enzymes play important roles in the metabolism of carbohydrates, amino acids, and cholesterol. Pyruvate carboxylase, a manganese-containing enzyme, and phosphoenolpyruvate carboxykinase (PEPCK), a manganese-activated enzyme, play critical roles in gluconeogenesis— the production of glucose from non-carbohydrate precursors. Arginase, another manganese-containing enzyme, is required by the liver for the urea cycle, a process that detoxifies ammonia generated during amino acid metabolism.

Bone development

Manganese deficiency results in abnormal skeletal development in a number of animal species. Manganese is the preferred cofactor of enzymes called glycosyltransferases, which are required for the synthesis of proteoglycans that are needed for the formation of healthy cartilage and bone.

Wound healing

Wound healing is a complex process that requires increased production of collagen. Manganese is required for the activation of prolidase, an enzyme that functions to provide the amino acid, proline, for collagen formation in human skin cells. A genetic disorder known as prolidase deficiency results in abnormal wound healing among other problems, and is characterized by abnormal manganese metabolism Glycosaminoglycan synthesis, which requires manganese-activated glycosyltranserases, may also play an important role in wound healing.

Nutrient interactions

Iron: Although the specific mechanisms for manganese absorption and transport have not been determined, some evidence suggests that iron and manganese can share common absorption and transport pathways. Absorption of manganese from a meal is reduced as the meal's iron content is increased. Iron supplementation (60 mg/day for 4 months) was associated with decreased blood manganese levels and decreased MnSOD activity in white blood cells, indicating a reduction in manganese nutritional status. An individual's iron status can affect manganese bioavailability. Intestinal absorption of manganese is increased during iron deficiency, and increased iron stores (ferritin levels) are associated with decreased manganese absorption. The finding that men generally absorb less manganese than women may be related to the fact that men usually have higher iron stores than women.

Magnesium: Supplemental magnesium (200 mg/day) decreased manganese bioavailability slightly, either by decreasing manganese absorption or by increasing its loss in healthy adults.

Calcium: In one set of studies, supplemental calcium (500 mg/day) resulted in slightly lower manganese bioavailability in healthy adults. As a source of calcium, milk had the least effect, while calcium carbonate and calcium phosphate had the greatest effect. Several others studies have found the effect of supplemental calcium on manganese metabolism to be minimal.

DEFICIENCY

Manganese deficiency has been observed in a number of animal species. Signs of manganese deficiency include impaired growth, impaired reproductive function, skeletal abnormalities, impaired glucose tolerance, and altered carbohydrate and lipid metabolism. In humans, demonstration of a manganese deficiency syndrome has been less clear. A child on long-term total parenteral nutrition (TPN) that lacked manganese developed bone demineralization and impaired growth that were corrected by manganese supplementation. Young men who were fed a low-manganese diet developed decreased serum cholesterol levels and a transient skin rash. Blood calcium, phosphorus, and alkaline phosphatase levels were also elevated, which may indicate increased bone remodeling as a consequence of insufficient dietary manganese. Young women fed a manganese-poor diet developed mildly abnormal glucose tolerance in response to an intravenous (IV) infusion of glucose.

By Lillian Waugh

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